Focusing on isolated, small muscle exercise effectively combats exercise intolerance in patients with chronic heart failure (CHF), according to a study conducted by an Italian and American research team and published in the Journal of the American College of Cardiology (JACC). This type of exercise promotes better oxygen transport, overcoming the central limitation of the impaired cardiac function, which may have significant implications for improving the quality of life for people with CHF.

Regular exercise in patients with CHF has previously been demonstrated to reduce symptoms, hospitalizations and disability, yet a defining characteristic of the condition remains diminished exercise capacity. While previous studies have revealed that exercising small muscle groups can provide health benefits without putting excess stress on the heart, these analyses have not documented how this occurs.

Seeking to answer this question, a research team from the University of Milan, the University of Utah, and the University of California, San Diego, analyzed the muscle structure, oxygen transport and metabolism of CHF patients before and after conducting an 8-week program of isolated, small muscle exercise. Specifically, the team enrolled 6 male patients with CHF and 6 healthy male control subjects matched by age, sex, and physical activity. The researchers then conducted a series of tests on the 12 men while they performed cycling exercises (whole-body exercise) and knee-extensor exercises (small-muscle mass exercise). Study participants with CHF subsequently underwent an 8-week training program of knee-extensor exercises (on a purposely designed dynamic ergometer) and were tested again at its completion to determine how their test results had changed.

The research team found that cardiac output during the knee-extensor exercise was not significantly different between the patients with CHF and the controls; neither was it significantly different before and after the 8 weeks of training. The researchers did find a change, however, in the amount of oxygen delivered to the leg muscles, due to a better blood flow redistribution. Before the training, the maximum amount of oxygen delivered to the leg muscles was significantly lower in the men with CHF than in the control subjects (at 0.53 ± 0.03 and 0.7 ± 0.04 l/min, respectively). After the training, however, the amount of oxygen delivered increased by approximately 54 percent in the CHF group, making the two groups equal. Consequently, maximum leg oxygen consumption increased by approximately 53 percent in the CHF group after the training, reaching a level significantly greater than the controls (0.60 ± 0.07 and 0.49 ± 0.03 l/min, respectively).

The researchers were able to correlate the CHF group’s training-induced improvement to changes in muscle structure, such as the growth of new blood vessels and the generation of additional mitochondria.

According to lead study author Fabio Esposito, MD, the responses are encouraging “as they indicate that the skeletal muscle of patients with CHF still has the potential to adapt in the expected fashion, if given the appropriate stimuli.” The research team concluded that their better understanding of the mechanisms responsible for these adaptations, “may have important practical consequences in terms of guiding future pharmacological and rehabilitative interventions in [the CHF] population.”

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